Chlordecone became widely recognized as a neurotoxicant when, in 1975, several individuals received high level acute exposure in a factory in Hopewell, Virginia. We are investigating the CNS mechanisms contributing to chlordecone's production of tremors and reproductive dysfunction. The effects of chlordecone poisoning on neurotransmitter receptor binding site density, levels, and turnover; and levels of neuroactive peptides are being examined. Pituitary gonadotrophins and steroid hormone levels are being measured to assess the contribution of neuroendocrine changes to the neurotoxicity of chlordecone, and peripheral and central indices of reproductive function are being assessed. In addition, the interaction of chlordecone with the estrogen receptor is being measured and the effect of estrogen on symptoms of chlordecone neurotoxicity are being examined. Finally, the regional and subcellular distribution of chlordecone in the CNS is being studied.